ArticleMolecular oncology2013
The HER2 amplicon includes several genes required for the growth and survival of HER2 positive breast cancer cells.
Article in Molecular oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 2 of them syntheses that pooled it.
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Who cites it
60 citing papers in PubMed, 2 syntheses or guidelines pooled it, 92 citations in OpenAlex.
- Meta-analysis identifies key genes and pathways implicated in Benzo[a]pyrene exposure response.Chemosphere · 2024Pooled it
- Agnostic Pathway/Gene Set Analysis of Genome-Wide Association Data Identifies Associations for Pancreatic Cancer.Journal of the National Cancer Institute · 2019Pooled it
- Adjusting breast cancer patient prognosis with non-HER2-gene patterns on chromosome 17.PloS one · 2014Trial
- StarD5 Regulates Cholesterol Homeostasis to Promote Colorectal Cancer Progression and the Cancer Stem Cell Phenotype.Molecular cancer research : MCR · 2026Article
- Single-cell multimodal profiling of pan-cancer cell lines uncovers gene regulatory principles underlying intrinsic cell states and environmental features.Nature communications · 2026Article
- HER2∆16 directs luminal cell identity and estrogen receptor signaling in HER2+ breast cancer.Nature communications · 2026Article
- Single-cell multimodal profiling of pan-cancer cell lines uncovers gene regulatory principles underlying intrinsic cell states and environmental features.bioRxiv : the preprint server for biology · 2026Article
- The lipid transfer protein STARD7 controls intestinal tumor development in a context-dependent manner.EMBO molecular medicine · 2026Article
- ERBB2 amplification is a late event in the pathogenesis of high-grade endometrial carcinomas with heterogeneous HER2 expression.The Journal of pathology · 2026Article
- Ketoboronate as a Minimal Covalent-Reversible Tag for Targeted Lysosomal Degradation of Extracellular and Membrane Proteins.Journal of the American Chemical Society · 2025Article
- A network model for patient-derived drug response in breast cancer integrating multi-omics datasets.bioRxiv : the preprint server for biology · 2025Article
- Article
- Is STARD3 A New Biomarker for Breast Cancer?European journal of breast health · 2024Review
- Characteristics of HPV integration in cervical adenocarcinoma and squamous carcinoma.Journal of cancer research and clinical oncology · 2023Article
- SMARCA4 and SMARCE1 in gastric cancer: Correlation with ARID1A, and microsatellite stability, and SMARCE1/ERBB2 co-amplification.Cancer medicine · 2023Article
- STARD3: A New Biomarker in HER2-Positive Breast Cancer.Cancers · 2023Article
- StAR-related lipid transfer domain protein 3 (STARD3) regulates HER2 and promotes HER2-positive breast cancer progression through interaction with HSP90 and SRC signaling.American journal of cancer research · 2023Article
- Whole-exome sequencing in moyamoya patients of Northern-European origin identifies gene variants involved in Nitric Oxide metabolism: A pilot study.Brain & spine · 2023Article
- Immunotherapy for HER-2 positive breast cancer.Frontiers in oncology · 2023Review
- Review
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
About 20% of breast cancers are characterized by amplification and overexpression of the HER2 oncogene. Although significant progress has been achieved for treating such patients with HER2 inhibitor trastuzumab, more than half of the patients respond poorly or become resistant to the treatment. Since the HER2 amplicon at 17q12 contains multiple genes, we have systematically explored the role of the HER2 co-amplified genes in breast cancer cell growth and their relation to trastuzumab resistance. We integrated aCGH data of the HER2 amplicon from 71 HER2 positive breast tumors and 10 cell lines with systematic functional RNA interference analysis of 23 core amplicon genes with several phenotypic endpoints in a panel of trastuzumab responding and non-responding HER2 positive breast cancer cells. Silencing of HER2 caused a greater growth arrest and apoptosis in the responding compared to the non-responding cell lines, indicating that the resistant cells are inherently less dependent on the HER2 pathway. Several other genes in the amplicon also showed a more pronounced effect when silenced; indicating that expression of HER2 co-amplified genes may be needed to sustain the growth of breast cancer cells. Importantly, co-silencing of STARD3, GRB7, PSMD3 and PERLD1 together with HER2 led to an additive inhibition of cell viability as well as induced apoptosis. These studies indicate that breast cancer cells may become addicted to the amplification of several genes that reside in the HER2 amplicon. The simultaneous targeting of these genes may increase the efficacy of the anti-HER2 therapies and possibly also counteract trastuzumab resistance. The observed additive effects seem to culminate to both apoptosis and cell proliferation pathways indicating that these pathways may be interesting targets for combinatorial treatment of HER2+ breast cancers.
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